中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
Chinese Journal of Anesthesiology
2015年
8期
951-954
,共4页
杨艳妮%冷玉芳%郑贯峥%吕兴华%苏玉洁%王朋
楊豔妮%冷玉芳%鄭貫崢%呂興華%囌玉潔%王朋
양염니%랭옥방%정관쟁%려흥화%소옥길%왕붕
青风藤属%肾%再灌注损伤%NF-κB%一氧化氮合酶Ⅱ型
青風籐屬%腎%再灌註損傷%NF-κB%一氧化氮閤酶Ⅱ型
청풍등속%신%재관주손상%NF-κB%일양화담합매Ⅱ형
Sinomenium%Kidney%Reperfusion injury%NF-kappa B%Nitric oxide synthase type Ⅱ
目的 探讨青藤碱对大鼠肾缺血再灌注时NF-KB及诱导型一氧化氮合酶(iNOS)水平的影响.方法 健康成年雄性Wistar大鼠72只,6～9周龄,体重180～220 g,采用随机数字表法分4组(n=18):对照组(C组)、青藤碱组(SIN组)、肾缺血再灌注组(I/R组)和青藤碱+肾缺血再灌注组(SIN+I/R组).采用夹闭左肾肾蒂45 min,再灌注即刻切除右肾的方法制备肾缺血再灌注损伤模型.SIN+I/R组再灌注前30 min、SIN组于相应时点腹腔注射青藤碱60 mg/kg.于再灌注6、8和12h时,心脏穿刺采集血标本,测定血清Cr和BUN浓度.取左肾组织,光镜下观察肾脏病理学结果,采用非生物素二步免疫组织化学法检测大鼠肾脏NF-KB阳性细胞率及iNOS的表达.结果 与C组比较,I/R组和SIN+I/R组血清Cr和BUN浓度升高,肾组织NF-KB阳性细胞率升高,iNOS表达上调(P＜0.05),SIN组上述指标差异无统计学意义(P＞0.05);与I/R组比较,SIN+I/R组血清Cr和BUN浓度降低,肾组织NF-κB阳性细胞率降低,iNOS表达下调(P＜0.05).SIN+I/R组肾组织病理学损伤较I/R组减轻.结论 青藤碱减轻大鼠肾缺血再灌注损伤的机制与抑制NF-KB活性,下调iNOS表达有关.
目的 探討青籐堿對大鼠腎缺血再灌註時NF-KB及誘導型一氧化氮閤酶(iNOS)水平的影響.方法 健康成年雄性Wistar大鼠72隻,6～9週齡,體重180～220 g,採用隨機數字錶法分4組(n=18):對照組(C組)、青籐堿組(SIN組)、腎缺血再灌註組(I/R組)和青籐堿+腎缺血再灌註組(SIN+I/R組).採用夾閉左腎腎蒂45 min,再灌註即刻切除右腎的方法製備腎缺血再灌註損傷模型.SIN+I/R組再灌註前30 min、SIN組于相應時點腹腔註射青籐堿60 mg/kg.于再灌註6、8和12h時,心髒穿刺採集血標本,測定血清Cr和BUN濃度.取左腎組織,光鏡下觀察腎髒病理學結果,採用非生物素二步免疫組織化學法檢測大鼠腎髒NF-KB暘性細胞率及iNOS的錶達.結果 與C組比較,I/R組和SIN+I/R組血清Cr和BUN濃度升高,腎組織NF-KB暘性細胞率升高,iNOS錶達上調(P＜0.05),SIN組上述指標差異無統計學意義(P＞0.05);與I/R組比較,SIN+I/R組血清Cr和BUN濃度降低,腎組織NF-κB暘性細胞率降低,iNOS錶達下調(P＜0.05).SIN+I/R組腎組織病理學損傷較I/R組減輕.結論 青籐堿減輕大鼠腎缺血再灌註損傷的機製與抑製NF-KB活性,下調iNOS錶達有關.
목적 탐토청등감대대서신결혈재관주시NF-KB급유도형일양화담합매(iNOS)수평적영향.방법 건강성년웅성Wistar대서72지,6～9주령,체중180～220 g,채용수궤수자표법분4조(n=18):대조조(C조)、청등감조(SIN조)、신결혈재관주조(I/R조)화청등감+신결혈재관주조(SIN+I/R조).채용협폐좌신신체45 min,재관주즉각절제우신적방법제비신결혈재관주손상모형.SIN+I/R조재관주전30 min、SIN조우상응시점복강주사청등감60 mg/kg.우재관주6、8화12h시,심장천자채집혈표본,측정혈청Cr화BUN농도.취좌신조직,광경하관찰신장병이학결과,채용비생물소이보면역조직화학법검측대서신장NF-KB양성세포솔급iNOS적표체.결과 여C조비교,I/R조화SIN+I/R조혈청Cr화BUN농도승고,신조직NF-KB양성세포솔승고,iNOS표체상조(P＜0.05),SIN조상술지표차이무통계학의의(P＞0.05);여I/R조비교,SIN+I/R조혈청Cr화BUN농도강저,신조직NF-κB양성세포솔강저,iNOS표체하조(P＜0.05).SIN+I/R조신조직병이학손상교I/R조감경.결론 청등감감경대서신결혈재관주손상적궤제여억제NF-KB활성,하조iNOS표체유관.
Objective To investigate the effect of sinomenine on the levels of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-two healthy male Wistar rats, aged 6-9 weeks, weighing 180-220 g, were randomly assigned into 4 groups (n =18 each) using a random number table: control group (group C), sinomenine group (group SIN), group I/R, and sinomenine+I/R group (group SIN+I/R).The animals were anesthetized with 10％ chloral hydrate 350 mg/kg.The left renal pedicles were clamped with atraumatic microclips for 45 min followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion to establish the model of renal I/R injury.Sinomenine 60 mg/kg was injected intraperitoneally at 30 min before reperfusion in group SIN +I/R, and at the corresponding time point in group SIN.At 6, 8 and 12 h of reperfusion, the blood samples were drawn by cardiac puncture for measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The left renal specimens were obtained for examination of pathological changes (with light microscopes) and for determination of the rate of NF-κB-positive cells and iNOS expression in renal tissues (by immunohistochemistry).Results Compared with group C, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly increased, and the expression of iNOS was up-regulated in I/R and SIN+I/R groups, and no significant change was found in the parameters mentioned above in group SIN.Compared with group I/R, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly decreased, and the expression of iNOS was down-regulated in group SIN+I/R.The microscopic examination showed that the pathological changes of kidney were significantly attenuated in group SIN+I/R compared with group I/R.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to inhibited activity of NF-κB and down-regulated expression of iNOS in rats.
